Our studies are directed at defining the role of cortical-NOT and cortical-DLPN pathways in the control of smooth pursuit, OKN and gaze holding in visually-deprived monkeys compared to normally-reared monkeys. The visual and oculomotor systems are not mature at birth in either monkeys or humans. These systems develop in a synergistic fashion during the first few months of life. The visual system depends on the oculomotor system to hold the image of an object of interest relatively stable on the retina, to allow clear, high acuity vision. The oculomotor system relies on visual signals to provide error information for calibration of oculomotor output. If binocular visual experience is disrupted early in life, disorders in vision, gaze holding, eye alignment and eye movements follow. These disorders are permanent and difficult to treat. Our hypothesis is that visual afferent structures including the pretectal nucleus of the optic tract (NOT) and dorsolateral pontine nucleus (DLPN) will be defective in cases with pathological gaze holding and smooth pursuit eye movements. The NOT and DLPN depend on inputs from the middle temporal (MT) and medial superior temporal (MST) visual cortical areas for normal function. Our studies are designed to manipulate early coordinated binocular visual experience to provide an appropriate animal model to study alterations in oculomotor circuits associated with congenital cataracts and strabismus. Our preliminary data indicates that neurons in MT/MST and NOT are differentially sensitive to various forms of early visual deprivation. The neural substrate for latent nystagmus and defective smooth pursuit will be investigated using single unit recording in awake, behaving macaques. Eye movements will be measured precisely with an electromagnetic method. Completion of our studies will improve the diagnosis and treatment of disorders of vision, gaze holding and eye movements in children.